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CPR II Week 2 > Drugs Used in Cardiac Arrhythmias > Flashcards

Drugs Used in Cardiac Arrhythmias Flashcards

1
Q

What cardiac structures are involved with the fast action potential?

A

1) Ventricular cardiomyocytes
2) Atrial cardiomyocytes
3) Purkinje fibers

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2
Q

What cardiac structures are involved with the slow (pacemaker) action potential?

A

1) SA node cells

2) AV node cells

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3
Q

What occurs during phase 0 of the fast action potential?

During phase 1?

Phase 2?

Phase 3?

Phase 4?

A

0) Na+ channels open due to depolarization and Na+ enters the cells
1) K+ exits cells
2) Plateau phase results from K+ exiting cells offset by and Ca2+ entering
3) Ca2+ channels close and K+ begins to exit more rapidly resulting in repolarization
4) Resting membrane potential is gradually restored by Na+/K+ ATPase and the Na+/Ca2+ exchanger

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4
Q

What occurs during phase 4 of the slow (pacemaker) action potential?

During phase 0?

Phase 3?

A

4) Slow spontaneous depolarization via T-type Ca2+ channels
0) Upstroke of Action Potential via L-type Ca2+ channels
3) Repolarization by inactivation of calcium channels with increased K+ efflux

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5
Q

What are the functions of the class 1A drugs?

A

1) Block sodium channels

2) Block potassium channels

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6
Q

What are the class 1A drugs?

A

1) Quinidine
2) Procainamide
3) Disopyramide

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7
Q

Procainamide has what effect on the SA and AV nodes?

What is its clinical use?

What adverse effect is noted with it?

A

1) Depresses their activity
2) Sustained ventricular tachycardias and arrhythmias associated with MI
3) Lupus related side effects

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8
Q

Both Quinidine and disopyramide have what effect on the heart?

What is the clinical use of disopyramide?

A

1) Antimuscarinic effect

2) Recurrent ventricular arrhythmias

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9
Q

What adverse effect is seen with the class 1A drugs?

A

QT interval prolongation and induction of torsade de pointes arrhythmia and syncope

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10
Q

What is the function of the class 1B drugs?

A

Block sodium channels

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11
Q

Why do class 1B drugs not prolong action potential or QT duration on ECG like class 1A drugs do?

A

They do not block potassium channels

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12
Q

What are the class 1B drugs?

A

1) Lidocaine

2) Mexiletine

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13
Q

What is the clinical use of lidocaine?

What is the route of administration?

A

1) Stop ventricular tachycardia from acute MI

2) IV

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14
Q

What is the clinical use of Mexiletine?

What is the route of administration?

A

1) Ventricular arrhythmias

2) Oral

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15
Q

What are the functions of the class 1C drugs?

A

1) Block sodium channels

2) Block certain potassium channels

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16
Q

What are the class 1C drugs?

A

1) Flecainide

2) Propafenone

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17
Q

What are the clinical uses of flecainide?

A

1) In patients with normal hearts who have supraventricular arrhythmias
2) Refractory ventricular arrhythmias that are life threatening

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18
Q

What are the clinical uses of propafenone?

How is its effect on beta-blocking?

A

1) Supraventricular arrhythmias in patients without structural disease
2) Weak

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19
Q

What adverse effect is seen with the class 1C drugs?

A

Exacerbation of ventricular arrhythmias

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20
Q

Beta-Blockers (Class 2 drugs) have what effect on the pacemaker action potential?

A

1) Increased slope due to effects on If (funny current) and T-type Ca channels
2) Reduced threshold potential due to effect on L-type Ca channels

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21
Q

Beta blockers have what effect on the SA node?

On the AV node?

A

1) Decrease HR and increase RR interval

2) Decrease AV conduction and increase PR interval

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22
Q

What are the beta blockers used to Tx arrhythmias?

A

1) Propranolol

2) Esmolol

23
Q

What type of beta blocker is esmolol?

A

Short acting selective beta-1 blocker

24
Q

Which beta blocker is used as a continuous i.v. infusion, with rapid onset
and termination of its action?

A

Esmolol

25
Q

What are the actions of the class 3 drugs?

A

1) Block potassium channels

2) Prolong QT interval

26
Q

What are the class 3 drugs?

A

1) Amiodarone
2) Sotalol
3) Dofetilide
4) Ibutilide

27
Q

Besides blocking potassium channels what else does Amiodarone do?

What is its clinical use?

A

1) Blocks inactivated Na2+ channels and calcium channels

2) Recurrent ventricular tachycardia and atrial fibrillation

28
Q

What potentially fatal adverse effect is associated with amiodarone?

A

Pulmonary fibrosis

29
Q

Besides blocking potassium channels what else does Sotalol do?

What is its clinical use?

A

1) Non-selective beta blocker

2) Treatment of life-threatening ventricular arrhythmias

30
Q

What adverse effect is seen with sotalol?

A

Provokes torsade de pointes

31
Q

What do dofetilide and ibutilide specifically block?

What is its clinical use?

A

1) Rapid component of the delayed rectifier potassium current
2) Restore sinus rhythm in patients with atrial fibrillation

32
Q

What adverse effect is seen with dofetilide and ibutilide?

A

QT interval prolongation and increased risk of ventricular arrhythmias

33
Q

What are the actions of the class 4 drugs?

It is active in cells exhibiting what type of potential?

A

1) Block L-type Calcium channels

2) Pacemaker potential

34
Q

What effect do the class 4 drugs have on the pacemaker potential?

A

1) Decrease the slope of phase 0 depolarization

2) Increase L-type Ca2+ channel threshold potential

35
Q

What are the class 4 drugs?

A

1) Verapamil

2) Diltiazem

36
Q

What is the clinical use of verapamil and diltiazem?

A

Termination and prevention of paroxysmal supraventricular tachycardia

37
Q

Adenosine activates A1 adenosine receptor which is a?

It has what effect on ions?

What effect does it have on the AV node?

A

1) Gi coupled GPCR
2) Enhances potassium current and inhibits Ca2+ and Funny currents
3) Inhibits AV conduction and increases AV nodal refractory period

38
Q

What is the clinical use of adenosine?

A

Conversion to sinus rhythm in paroxysmal supraventricular tachycardia

39
Q

What is proarrhythmia?

A

Drug-induced significant new arrhythmia or worsening of an existing arrhythmia

40
Q

Which classes of drugs cause excessive slowing of repolarization which leads to torsades de pointes?

Which causes excessive slowing of conduction leading to persistent ventricular tachycardias?

A

1) Class 1A and Class 3 drugs

2) Class 1A and 1C drugs

41
Q

Atrial fibrillation is initiated and sustained due to formation of?

A

Reentry circuits

42
Q

Reentry is a type of arrhythmia in which?

A

One impulse re-enters and excites areas of the heart more than once

43
Q

What is the atrial activation rate in atrial fibrillation?

The ventricular rate?

A

1) 350-600 bpm

2) 120-180 bpm

44
Q

What is used to treat Afib?

A

Direct current cardioversion

45
Q

What drugs are used as chemical cardioversion in the treatment of Afib?

A

1) Class 1C agents

2) Class 3 agents

46
Q

How do class 1C agents terminate reentry in order to treat Afib?

Class 3 agents?

A

1) Block fast Na+ channel to reduce retrograde conduction through damaged tissue
2) Block K+ channels to keep cells in their refractory period

47
Q

What drugs are used in order to maintain sinus rhythm in AFib patients with structural heart disease?

A

The Class 3 drugs:

1) Sotalol
2) Amiodarone
3) Dofetilide

(Class 1C drugs are contraindicated in this case)

48
Q

What is the most common type of paroxysmal supraventricular tachycardia?

A

Atrioventricular nodal reentrant tachycardia

49
Q

What does paroxysmal supraventricular tachycardia look like on ECG?

A

1) Narrow QRS
2) Tachycardia
3) P wave inverted or hidden in QRS

50
Q

What drugs are used in the prevention of paroxysmal supraventricular tachycardia?

A

Class 4 drugs:
1) Verapamil and Diltiazem

Class 2 drugs:
2) Metoprolol and propranolol

51
Q

Torsade de pointes is often associated with impaired function of?

This leads to?

A

1) Potassium channels

2) Prolonged repolarization

52
Q

Torsade de pointes is associated with what syndrome?

A

Long QT syndrome

53
Q

What drugs can cause the form of Torsade de pointes known as acquired long QT syndrome?

A

1) Class 1A

2) Class 3 (Amiodarone excluded)

CPR II Week 2 (6 decks)

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